miR‐20a inhibits hypoxia‐induced autophagy by targeting ATG5/FIP200 in colorectal cancer

Che, Jing; Wang, Wenshan; Huang, Yu; Zhang, Lu; Zhao, Jing; Zhang, Peng; Yuan, Xianglin

doi:10.1002/mc.23006

Cited by 36 publications

(21 citation statements)

References 66 publications

(110 reference statements)

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“…Additionally, Zheng et al [ 35 ] suggested that ATG5 inhibition contributed to treatment for esophageal carcinoma patients. Furthermore, autophagy abolition through the ATG5/7 re-sensitized EC109/CDDP knockdown or the use of pharmacological inhibitors is greatly significant [ 36 ] not only in the esophageal, but also in gastric [ 37 ], colorectal [ 38 , 39 ], bladder [ 40 ], ovarian [ 41 ], and prostate cancers [ 42 ]. With regard to TBK1, it has been proven that TBK1 takes part in modulating cell growth and autophagy [ 43 ].…”

Section: Discussionmentioning

confidence: 99%

Prognostic significance of autophagy-related genes within esophageal carcinoma

Chen

Cao

et al. 2020

BMC Cancer

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Background: Several works suggest the importance of autophagy during esophageal carcinoma development. The aim of the study is to construct a scoring system according to the expression profiles of major autophagy-related genes (ARGs) among esophageal carcinoma cases. Methods: The Cancer Genome Atlas was employed to obtain the esophageal carcinoma data. Thereafter, the online database Oncolnc (http://www.oncolnc.org/) was employed to verify the accuracy of our results. According to our results, the included ARGs were related to overall survival (OS). Results: We detected the expression patterns of ARG within esophageal carcinoma and normal esophageal tissues. In addition, we identified the autophagy related gene set, including 14 genes displaying remarkable significance in predicting the esophageal carcinoma prognosis. The cox regression results showed that, 7 ARGs (including TBK1, ATG5, HSP90AB1, VAMP7, DNAJB1, GABARAPL2, and MAP2K7) were screened to calculate the ARGs scores. Typically, patients with higher ARGs scores were associated with poorer OS. Moreover, the receiver operating characteristic (ROC) curve analysis suggested that, ARGs accurately distinguished the healthy people from esophageal carcinoma patients, with the area under curve (AUC) value of > 0.6. Conclusion: A scoring system is constructed in this study based on the main ARGs, which accurately predicts the outcomes for esophageal carcinoma.

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Section: Discussionmentioning

confidence: 99%

Prognostic significance of autophagy-related genes within esophageal carcinoma

Chen

Cao

et al. 2020

BMC Cancer

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“…As we know, autophagy plays a vital role in various physiologic and pathologic processes containing tumorigenesis (15,16). ATG5, as one of the critical regulators of autophagy, can be regulated by various genes contributing to tumorigenesis, tumor progression, and chemo-/radio-resistance (8,(17)(18)(19)(20). However, the relation between ATG5 and CDKL3 in tumors was firstly revealed in our report.…”

Section: Discussionmentioning

confidence: 66%

CDKL3 Targets ATG5 to Promote Carcinogenesis of Esophageal Squamous Cell Carcinoma

et al. 2020

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Objective: Our previous study suggested cyclin-dependent kinase-like 3 (CDKL3) acts as a new oncogene in esophageal squamous cell carcinoma (ESCC) cell line TE-1. However, the molecular mechanisms and biological effects of CDKL3 in ESCC remain unknown. In the present study, we aimed to explore the clinical significance of CDKL3 in ESCC and how CDKL3 regulates the malignant behavior of ESCC. Methods: ESCC samples were stained by immunohistochemical staining (IHC) and analyzed for the expression of CDKL3. The functions of CDKL3 on proliferation, apoptosis, migration, invasion, and colony formation were investigated by celigo assay, MTT assay, colony formation, caspase 3/7 activity analysis, transwell migration and invasion assay, respectively. A transplanted tumor model was established to study the functions of FLVCR1 on the tumorigenesis of ESCC cells. Microarray analysis was utilized to identify the CDKL3-regulated genes in ESCC cells. Results: ESCC tumor tissues possessed a significantly higher expression of CDKL3 and autophagy-related gene 5 (ATG5) than matched adjacent normal tissues. The high expressions of CDKL3 were positively associated with the tumor-node-metastasis (TNM) stage and Ki67. Upregulated ATG5 expression was positively correlated with male, advanced tumor (T) stage, and TNM stage. Kaplan-Meier analysis showed that ESCC patients with higher expression of CDKL3 or ATG5 had a shorter overall survival. The worst prognosis was recognized in patients with both high manifestations of CDKL3 and ATG5. Time-dependent receiver operating characteristic (ROC) curve was established to reveal that the combination of CDKL3, ATG5, and TNM stage-based model had better prognostic accuracy than TNM stage. Moreover, CDKL3 knockdown markedly repressed cell growth and aggressivity in vitro and in vivo. Mechanistically, ATG5 was confirmed as a downstream gene involved in the pro-oncogenic function of CDKL3. Conclusion: CDKL3 can be utilized as an independent poor prognostic marker in ESCC patients. Furthermore, CDKL3 may promote tumor profession, invasion, metastasis, and prohibit tumor apoptosis partly by ATG5 activation.

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“…For example, hypoxia-induced autophagy promotes the occurrence and progression of CRC via the PRKC/PKC-EZR pathway ( 36 ). Che et al reported that miR-20a suppressed hypoxia-induced autophagy by targeting ATG5/FIP200 in CRC ( 37 ). Therefore, to gain a better under-standing of the molecular regulatory mechanisms underlying circCCDC66, the present study examined the association between miR-3140 and autophagy.…”

Section: Discussionmentioning

confidence: 99%

Hypoxia‑induced circCCDC66 promotes the tumorigenesis of colorectal cancer via the miR‑3140/autophagy pathway

Jin

Zhong

et al. 2020

Int J Mol Med

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Circular RNAs (circRNAs) have been reported to be involved in the progression of colorectal cancer (CRC). However, the biological role of circCCDC66 in CRC remains unclear. Therefore, the present study aimed to elucidate the mechanisms through which circCCDC66 affects the hypoxia-induced progression of CRC. It was found that hypoxia promoted the progression of CRC and upregulated the expression of circCCDC66. Furthermore, circCCDC66-knockdown reduced viability, migration and invasion, and enhanced the apoptosis of hypoxia-exposed CRC cells. Using the starBase database, it was identified that circCCDC66 may bind to miR-3140. Subsequently, it was confirmed that circCCDC66 serves as a sponge of miR-3140 and the depletion of miR-3140 partly abolished the effects of circCCDC66 on the phenotype of hypoxia-exposed CRC cells. In addition, miR-3140 was validated to inhibit the autophagy pathway. The use of an autophagy inducer partially reversed the miR-3140 overexpression-induced inhibition of the viability and invasion, and the promotion of the apoptosis of hypoxia-exposed CRC cells. In summary, the findings of the present study demonstrated that circCCDC66 facilitates the development of CRC cells under hypoxic conditions via regulation of miR-3140/autophagy. These findings may provide a novel therapeutic option for patients with CRC.

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miR‐20a inhibits hypoxia‐induced autophagy by targeting ATG5/FIP200 in colorectal cancer

Cited by 36 publications

References 66 publications

Prognostic significance of autophagy-related genes within esophageal carcinoma

Prognostic significance of autophagy-related genes within esophageal carcinoma

CDKL3 Targets ATG5 to Promote Carcinogenesis of Esophageal Squamous Cell Carcinoma

Hypoxia‑induced circCCDC66 promotes the tumorigenesis of colorectal cancer via the miR‑3140/autophagy pathway

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